According to a new study published in Nature, a research team from Yale has identified the mechanism by which alterations in gut bacteria leads to obesity.
The bacteria in obese mice produced high levels of acetate, which stimulated the secretion of insulin by beta cells in the pancreas. High levels of insulin promote the storage of blood sugar as fat and can lead to type-2 diabetes. Additionally, the acetate also stimulated the secretion of gastrin and ghrelin, causing an increase in food intake.
When the gut bacteria of obese mice were transplanted into non-obese mice, the researchers observed similar changes in acetate levels and insulin.